Cytochalasin E targets actin filaments, the key components of the cytoskeleton. It binds to the barbed end of actin filaments and prevents actin polymerization and elongation. By disrupting actin dynamics, it impairs cellular processes such as cell division, migration, and intracellular trafficking.

A549 cell proliferation is dramatically suppressed by cytochalasin E in a dose-dependent manner [3]. Cytochalasin E has the ability to upregulate SQSTM1/p62 and autophagy-related proteins (LC3-II) [3].

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In vitro, Cytochalasin E is a potent inhibitor of actin polymerization. It binds and caps the barbed end of actin filaments, preventing the addition of new actin monomers. It has been shown to inhibit angiogenesis and tumor cell growth. It also enhances the expression of the low-affinity Fc epsilon receptor (CD23).

In vivo, Cytochalasin E has been reported to inhibit angiogenesis and tumor growth. It has been studied in animal models of cancer. As a microfilament inhibitor, it disrupts the actin cytoskeleton and impairs cellular processes essential for tumor progression.

The in vitro actin polymerization assay for Cytochalasin E involves measuring the rate and extent of actin filament formation. Purified actin monomers are incubated with the compound, and polymerization is monitored using fluorescence or light scattering. The inhibition of actin elongation by Cytochalasin E is measured.

In vitro cell-based assays are performed using various cell lines. Cells are treated with Cytochalasin E, and the effects on the actin cytoskeleton are visualized using fluorescently labeled phalloidin. Cell migration, proliferation, and morphological changes are assessed. The compound's effects on angiogenesis are evaluated using endothelial cell tube formation assays.

In vivo animal experiments for Cytochalasin E have been conducted in models of cancer and angiogenesis. Animals are administered the compound via appropriate routes, and tumor growth, angiogenesis, and metastasis are assessed. The compound's effects on the actin cytoskeleton in vivo are evaluated by histological analysis.

Pharmacokinetic properties of Cytochalasin E are not well-characterized in the literature. As a fungal metabolite, it is known to be bioactive and has been studied for its biological effects. Detailed PK parameters such as half-life, clearance, and bioavailability are not readily available.

Toxicological data for Cytochalasin E indicate that it is a fungal toxin with potential cytotoxic effects. It is known to disrupt the actin cytoskeleton, which can lead to cell death. The compound is intended for research use only and not for therapeutic use in humans.

[1]. Cytochalasin E, an epoxide containing Aspergillus-derived fungal metabolite, inhibits angiogenesisand tumor growth. J Pharmacol Exp Ther. 2000 Aug;294(2):421-7.

[2]. Green tea extract modulates actin remodeling via Rho activity in an in vitro multistep carcinogenicmodel. Clin Cancer Res. 2005 Feb 15;11(4):1675-83.

[3]. Variation in the activity of distinct cytochalasins as autophagy inhibitiors in human lung A549 cells. Biochem Biophys Res Commun. 2017 Dec 16;494(3-4):641-647.

Cytochalasin E is a cytochalasin alkaloid that functions as a metabolite. It has been reported in Mariannaea elegans, fungi (Mycotypha), and other organisms with relevant data. Mechanism of Action: Major biological effects include blocking cytokinesis leading to multinucleated cell formation, inhibiting cell motility, and inducing nuclear ejection… Other reported effects include inhibition of glucose transport, thyroid secretion, growth hormone release, phagocytosis, platelet aggregation, and thrombus contraction. /Cytochalasin/ This study investigated the effects of cytochalasin B and E on the intestinal digestion of maltose and sucrose and their digestion products glucose and fructose in mice in vitro. In mouse jejunal eversion sacs, incubation with 5.0 and 10.0 μg/ml concentrations of cytochalasin B or E for 60 minutes did not affect the digestion of maltose or sucrose, nor the activity of maltase or sucrase. However, cytochalasin E (5.0 μg/ml) inhibited glucose uptake from maltose and sucrose digestion by 68.5% and 65.9%, respectively, while cytochalasin B at the same concentration inhibited glucose uptake by 29.5% and 13.1%, respectively. Cytochalasin B and E appear to stimulate fructose uptake from sucrose digestion in the mouse jejunum. The inhibitory effect of cytochalasin E on galactose uptake in the mouse jejunal fossa was investigated. When cytochalasin B was added to the mucosal solution, its inhibitory efficacy on galactose uptake was the highest, followed by cytochalasin E, A, C, and D. In mouse Y-1 adrenal tumor cells, cytochalasin E, D, B, and H2B inhibited steroid production and caused cell rounding by interfering with actin polymerization, rather than through effects unrelated to actin binding. For more complete data on the mechanisms of action of cytochalasin E (10 in total), please visit the HSDB record page.

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Cytochalasin E is a member of the cytochalasan alkaloid family and has been reported in various fungal species. It is a well-known tool compound for studying actin dynamics and cytoskeletal function. It has been used in research to investigate cell division, migration, and intracellular trafficking. It is not approved for clinical use.

C28H33NO7

495.5641

495.225

36011-19-5

36011-19-5 (Cytochalasin E); 22144-77-0 (Cytochalasin D)

5458385

White to off-white solid powder

1.3±0.1 g/cm3

705.1±60.0 °C at 760 mmHg

206ºC

380.2±32.9 °C

0.0±2.4 mmHg at 25°C

1.608

1.92

2

7

2

36

986

9

C[C@H]1C/C=C/[C@H]2[C@H]3[C@](O3)([C@H]([C@@H]4[C@]2(C(=O)N[C@H]4CC5=CC=CC=C5)OC(=O)O/C=C/[C@@](C1=O)(C)O)C)C

LAJXCUNOQSHRJO-KGDUIROVSA-N

InChI=1S/C28H33NO7/c1-16-9-8-12-19-23-27(4,35-23)17(2)21-20(15-18-10-6-5-7-11-18)29-24(31)28(19,21)36-25(32)34-14-13-26(3,33)22(16)30/h5-8,10-14,16-17,19-21,23,33H,9,15H2,1-4H3,(H,29,31)/b12-8+,14-13+/t16-,17-,19-,20-,21-,23-,26+,27+,28?/m0/s1

(1E,4S,6R,7E,14S,14aS,15S,15aR,16aS,16bS)-14-benzyl-6-hydroxy-4,6,15,15a-tetramethyl-3,13,14,14a,15,15a,16a,16b-octahydro-[1,3]dioxacyclotridecino[4,5-d]oxireno[2,3-f]isoindole-5,10,12(4H,6H)-trione

NSC-175151; NSC 175151; NSC175151

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)